Abstract

Background: Postoperative Rathke cleft cyst surgery can cause injury to the pituitary gland or impaired secretion of antidiuretic hormone (ADH), leading to central diabetes insipidus (DI). This case report describes the successful postoperative management of DI in pediatric patients with Rathke’s cleft cyst who underwent transsphenoidal endonasal tumor surgery.

Case Description: An 8-year-old girl with diabetes insipidus (DI) following transsphenoidal endonasal surgery for a Rathke’s cleft cyst was admitted to the intensive care unit (ICU) for postoperative management. Initially, the patient received oxytocin infusion at 20 mU/min. Between the 13th and 15th hour postoperatively, urine output increased to 100–200 mL/h (5–10 mL/kgBW/h). In response, oral desmopressin therapy was initiated at a dose of 0.05 mg once daily. Twelve-hour evaluations showed stable urine output at approximately 500 mL/h (2.5 mL/kgBW/h). Based on this, the decision was made to discontinue oxytocin and prepare for transfer to the high care unit (HCU). In the HCU, urine output was monitored every 24 hours, and oral desmopressin was continued at the same dosage. On the third day of treatment, urine output increased significantly to 6400 mL/24 h (14.03 mL/kgBW/h). Consequently, the desmopressin dose was increased to 0.05 mg twice daily. This adjusted therapy was maintained. By the fifth day, urine output began to decrease, reaching 6 mL/kgBW/h.

Conclusion: Postoperative management of DI using desmopressin therapy yields favorable outcomes during both intensive care and high-care treatment in pediatric patients undergoing transsphenoidal endonasal surgery for Rathke’s cleft cyst.

Keywords: Diabetes insipidus, Endonasal, Pediatric, Rathke’s cleft cyst, Suprasellar tumor, Transsphenoidal

INTRODUCTION

Diabetes insipidus (DI) is a disorder characterized by the kidneys’ inability to conserve body water, resulting in polyuria (excessive urine output) and polydipsia (excessive thirst). It arises due to either a deficiency of or resistance to antidiuretic hormone (ADH), which is essential for maintaining the body’s fluid balance. DI is classified into two main types: Central (neurogenic) DI, caused by insufficient secretion of ADH from the pituitary gland, and nephrogenic DI, which occurs when the kidneys fail to respond appropriately to ADH. The global prevalence of DI is estimated at approximately 1 in 25,000 people. In children, the prevalence is even lower, with the central type being the most commonly diagnosed form. If not properly managed, DI can lead to serious complications, including severe dehydration and electrolyte imbalances.[ 7 , 11 ]

Clinical symptoms of DI in pediatric patients commonly include polyuria, characterized by excessive urine output that can reach 3–5 liters per day, and polydipsia, or excessive thirst, prompting the child to consume unusually large amounts of fluid. Children with DI frequently present signs of dehydration, such as dry mouth, dry skin, and weight loss. In more severe cases, persistent dehydration can lead to electrolyte imbalances, most notably hypernatremia. This condition poses serious risks, including seizures, confusion, and, in extreme cases, coma. These symptoms typically develop progressively and can worsen rapidly if not promptly treated.[ 1 , 11 ]

Rathke’s cleft cyst (RCC) is a benign, cystic lesion that arises from remnants of Rathke’s pouch, an embryonic precursor involved in the development of the pituitary gland. These cysts are typically located in the sellar region, adjacent to the pituitary, and are usually filled with clear or mucinous fluid. RCCs are generally classified into two categories based on size and clinical presentation: Asymptomatic cysts, which are often incidentally discovered during brain imaging. Symptomatic cysts, which may cause visual disturbances, hormonal imbalances, or neurological symptoms due to compression of surrounding structures. The global prevalence of RCC is estimated to be 0.2–0.5% based on brain imaging studies in the general population, though the majority of cases remain clinically silent. In pediatric populations, RCC is relatively rare but may be identified in children presenting with endocrine abnormalities or neurological complaints.[ 13 ]

Surgically, the primary challenge in managing RCC lies in its proximity to critical structures, such as the pituitary gland and optic nerve. This anatomical positioning necessitates high surgical precision and expertise to prevent damage to endocrine function and visual pathways. The transsphenoidal approach is commonly employed ,however, the procedure still carries potential risks, including cerebrospinal fluid (CSF) leakage, infection, and intraoperative bleeding. Perioperative management also poses challenges, particularly in maintaining hormonal balance, as RCC can disrupt pituitary function. Therefore, conducting a comprehensive hormonal evaluation both pre- and postoperatively is crucial.[ 3 , 5 ]

After RCC surgery, either by a transsphenoidal approach or other procedures, injury to the pituitary gland or impaired secretion of ADH can lead to central DI, leading to excessive urine production and the risk of dehydration and electrolyte imbalances, especially hypernatremia. The main challenges of intensive care unit (ICU) care include proper fluid volume regulation, as children with postoperative DI tend to experience significant fluid loss through the urine. This management requires close monitoring of fluid input and output, as well as careful correction of electrolytes to prevent complications such as seizures or organ damage due to sodium imbalance. In addition, ADH replacement therapy, either with desmopressin or other therapies, is often necessary to control DI symptoms and optimize fluid balance. Regular laboratory monitoring to assess sodium levels, plasma osmolarity, and kidney function is also an integral part of ICU care.[ 9 ]

CASE REPORT

An 8-year-old girl with a body weight of 20 kg, height of 110 cm, and a body mass index (BMI) of 16.5 kg/m² was diagnosed with a suprasellar tumor—suspected Rathke’s cleft cyst—presenting with bitemporal hemianopsia and compressive optic neuropathy in the left eye (oculi sinistra), likely due to a chiasmal lesion. She subsequently underwent a tumor excision procedure.

From the anamnesis, the patient was reported by her parents to have experienced progressive vision loss over the past two years, which has gradually worsened. This was accompanied by dizziness and short stature not in accordance with age-related growth expectations. Additionally, the patient exhibited frequent disorganized behavior and reported excessive thirst. There was no history of seizures, nausea, or vomiting.

Preoperative Physical Examination:

Airway: Patent, spontaneous breathing

Respiratory rate: 18 breaths/min Oxygen saturation (SpO2): 98%

Breath sounds: Vesicular (+/+), no rhonchi or wheezing

Mallampati classification: Grade 2

Mouth opening: Three fingers

Thyromental distance: 6 cm

Neck mobility: Full flexion and extension without restriction

Acral condition: Red, dry, warm; Capillary refill time (CRT): < 2 seconds

Blood pressure: 126/92 mmHg

Pulse: 92 beats/min, regular, strong

Heart sounds: Single S1/S2

Glasgow Coma Scale (GCS): 15 (score: 4-5-6)

Visual acuity: Right eye (OD) 6/6, left eye (OS) 0.5/60

Microphone sounds: Spontaneous and frequent Body temperature: 36.7°C

Preoperative Laboratory Evaluation:

Routine laboratory results showed the following values:

Hemoglobin (Hb): 11.2 g/dL

Leukocyte count: 8,460/μL

Hematocrit: 32.7%

Platelet count: 319,000/μL

Sodium: 138 mmol/L

Potassium: 4.33 mmol/L

Chloride: 102 mmol/L

Partial thromboplastin time (PT): 13.4/11.6

International normalized ratio (INR): 1.32

Activated partial thromboplastin time (aPTT): 43.7/26.1

Albumin: 4.88 g/dL

SGOT (AST): 31 U/L

SGPT (ALT): 16 U/L

Urea: 33.1 mg/dL

Creatinine: 0.46 mg/dL

Total T3: 0.53 ng/mL (reference range: 0.8–2.0 ng/mL)

Free T4: 0.47 ng/dL (reference range: 0.93–1.7 ng/dL)

TSH (Thyroid-Stimulating Hormone): 2.05 μIU/mL (reference range: 0.270–4.20 μIU/mL)

Prolactin: 205 μIU/mL (reference range: 102–496 μIU/mL)

Cortisol: 47.36 μIU/mL

Radiological findings:

Chest X-ray (Thorax): No abnormalities were observed; cardiac silhouette and pulmonary fields were within normal limits.

Computed Tomography (CT) Scan (Brain):

Revealed an extra-axial cystic mass with calcified components located in the intra- and suprasellar regions. The appearance raised suspicion of craniopharyngioma or a Rathke’s cleft cyst. No pathological lesions were detected within the brain parenchyma.

Magnetic Resonance Imaging (MRI) of the Brain:

Identified intra- and suprasellar cystic lesions with high protein content and rim calcification (+). The lesion appeared to compress the optic chiasm, supporting the diagnosis of a Rathke’s cleft cyst.

The patient was classified as ASA Physical Status III (American Society of Anesthesiologists). The case involved a pediatric patient with a suprasellar tumor, suspected to be a Rathke’s cleft cyst, associated with left eye (OS) vision loss, hypothyroidism, and polyuria, raising suspicion of DI.

Prior to induction, hemodynamic monitoring was established. The patient received sedation with Midazolam 2 mg IV bolus and analgesia with Fentanyl 50 mcg IV. General anesthesia was induced using Propofol 50 mg IV, and neuromuscular blockade was achieved with Atracurium 10 mg IV to facilitate endotracheal intubation. Following successful intubation, mechanical ventilation was initiated via an anesthesia machine, using pressure control mode with a target tidal volume of 5–8 mL/kg body weight. A central venous catheter (CVC) was inserted via the right subclavian vein (dextra subclavia) after induction.

The patient was placed in the supine position for the procedure. Anesthesia was maintained with a continuous infusion of Propofol at 15–50 mcg/kg/min, Atracurium at 5 mg/h, and Fentanyl at 10 mcg/h. Additional intraoperative medications included Tranexamic Acid 500 mg IV and Ondansetron 4 mg IV.

The surgery was performed using an endonasal transsphenoidal approach, with a total operative time of 7 hours. Intraoperative blood loss was approximately 125 cc, and urine output was 1075 cc. The patient received 1000 cc of balanced intravenous fluids and 200 cc of packed red cells (PRC).

Throughout the surgery, hemodynamic parameters remained stable, with no episodes of hypotension or shock. The heart rate was stable without tachycardia, and core body temperature was maintained between 35–35.5°C.

During the procedure, a cystic tumor was identified in the suprasellar region. The cystic content appeared mucous and light yellow in color, and successful drainage of the fluid was achieved, followed by closure of the dura [ Figure 1 and Table 1 ].

Figure 1:

Cystic lesions filled with mucous fluid.

Table 1:

Monitoring during operation.

Within the first hour of surgery, the patient exhibited polyuria, with urine output reaching 425 mL/h (21.25 mL/kg body weight/hour). In response, continuous intravenous oxytocin at 20 mU/min was initiated. Despite an initial fluid bolus of 300 mL, urine output remained fluctuant throughout the 5-hour procedure, requiring ongoing titration of oxytocin between 10 and 20 mU/min, alongside intraoperative fluid adjustments based on urinary output.

As the patient remained hemodynamically stable without any episodes of shock, early emergence from anesthesia was performed, and the patient was transferred to the Intensive Care Unit (ICU) for continued postoperative management.

Upon admission to the ICU, the patient was conscious with a Glasgow Coma Scale (GCS) score of E4V5M6. Vital signs were stable: blood pressure ranged from 120–134/60–72 mmHg, pulse rate between 80–92 bpm, respiratory rate at 18–20 breaths/min, and oxygen saturation (SpO₂) at 99–100% under non-rebreather mask (NRBM) oxygen at 8–10 L/min. Continuous oxytocin infusion at 20 mU/min was maintained, and hourly urine output monitoring was initiated [ Table 2 ].

Table 2:

Postoperative monitoring.

During the first 10 hours, urine output averaged 50 mL/h (2.5 mL/kg BW/h). However, between the 13th and 15th hour, urine output increased significantly to 100–200 mL/h (5–10 mL/kg BW/h). In response, oral desmopressin therapy was initiated at 0.05 mg once daily.

Subsequent 12-hour evaluations indicated stable urine output at approximately 500 mL/h (2.5 mL/kg BW/h). Given the stabilized condition, the oxytocin infusion was discontinued, and preparations were made for the patient’s transfer to the High Care Unit (HCU).

Postoperative Supportive Examination and Management:Post-surgical laboratory evaluations revealed:

Hemoglobin: 8.4 g/dL

Leukocyte count: 6,600/μL Hematocrit: 25.8%

Platelets: 219,000/μL

Plasma Electrolytes: Sodium 139 mmol/L, Potassium 4.33 mmol/L, Chloride 108 mmol/L

Urine Electrolytes: Sodium 144.9 mmol/L, Potassium 69.4 mmol/L, Chloride 179.5 mmol/L

Albumin: 3.78 g/dL

Urea: 25.2 mg/dL

Creatinine: 0.51 mg/dL

Random Blood Glucose (GDS): 103 mg/dL

Medications administered postoperatively included:

IV Tranexamic Acid 250 mg every 8 hours for 24 hours

IV Ondansetron 4 mg every 12 hours

IV Paracetamol 500 mg every 8 hours for analgesia

Continuous IV Fentanyl infusion at 10 mcg/h

Postoperative CT Scan Findings:

An isodense extra-axial lesion (density 19–24 HU) with calcified components located in the suprasellar region.

Estimated lesion dimensions:

Axial Plane: Anteroposterior (AP) 1.3 cm × Craniocaudal (CC) 1.1 cm × Laterolateral (LL) 0.8 cm

Overall volume impression: ~2.9 × 2.2 × 3.6 cm

The lesion exerted anterior compression on the optic chiasm.

Postoperative bony defects were observed in the superior wall of both sphenoid sinuses and sella turcica, consistent with surgical intervention.

Day 1 in HCU:

Urine output: 2050 mL/24 h (~4.49 mL/kgBW/h)

Oral desmopressin: Continued at 0.05 mg once daily

Patient education: Encouraged to maintain adequate oral hydration

Day 3:

Significant polyuria observed: 6400 mL/24 h (~14.03 mL/kgBW/h)

Hemodynamics: Stable

Oral intake: Frequent drinking observed

Management:Desmopressin increased to 0.05 mg twice daily

Close monitoring continued in HCU

Plasma electrolytes:

Sodium: 162 mmol/L (↓ severe hypernatremia)

Potassium: 2.77 mmol/L (↓ mild hypokalemia) Chloride: 121 mmol/L (↓)

Day 4:

Urine output: 6500 mL/24 h (~14.2 mL/kgBW/h) — still elevated

Electrolytes: Sodium: 146 mmol/L (↓ improving)

Potassium: 2.53 mmol/L (↓ further)

Chloride: 107 mmol/L (↓ improving)

Management:

Desmopressin: Continued at current dose

Hydration and electrolyte balance monitored Continued education on adequate fluid intake

Day 5:

Urine output decreased to ~6 mL/kgBW/h — showing response to therapy

DISCUSSION

The pituitary gland is situated within the sella turcica, directly beneath the optic nerves, optic chiasm, and optic tracts, making it susceptible to compressive visual impairment if a mass develops in this region. Functionally, the pituitary gland plays a central role in regulating various endocrine organs, including the thyroid gland, adrenal glands, ovaries, and testes. It also controls essential physiological processes such as lactation, uterine contractions, linear growth and development, and intravascular fluid homeostasis by promoting water reabsorption in the kidneys.

Tumors in the pituitary region can therefore lead to a range of hormonal deficiencies, including hypothyroidism, hypoprolactinemia, and hypocortisolism, as well as visual disturbances. Surgical intervention is typically indicated in cases of progressive visual loss, hypopituitarism, or if the tumor is associated with hemorrhage or abscess formation. However, surgical removal of pituitary tumors can also compromise pituitary function, particularly antidiuretic hormone (ADH) secretion, potentially leading to central diabetes insipidus (DI).[ 3 ]

In this case, the patient experienced a gradual decline in vision over the past two years. The left eye presented with visual impairment, and the right eye showed blurriness. An ophthalmological examination revealed optic atrophy in the left eye and lesions in the right eye. Radiological imaging confirmed the presence of cystic lesions in the suprasellar region, which were exerting pressure on the optic chiasm. Hormonal evaluations revealed hypothyroidism and hypocortisolism, although these were not followed up adequately. Additionally, the patient exhibited growth disturbances, but growth hormone levels were not evaluated at that time. Given the progressive visual impairment and the risk of further damage, the decision was made to proceed with surgical intervention to preserve the remaining vision.

Perioperative management involves careful preoperative assessment, anesthesia management during surgery, and postoperative care. The preoperative assessment primarily focuses on evaluating the impact of the suprasellar tumor on surrounding structures, especially the optic chiasm, which can lead to visual impairment. Symptoms and signs in patients with a mass in the sella can manifest as either functional or non-functional abnormalities: Functional masses tend to present with symptoms of hormonal excess (e.g., excess prolactin or cortisol). Non-functional masses, such as Rathke’s cleft cyst (RCC), typically cause mass effect symptoms. These may include headaches, vision loss due to pressure on the optic chiasm, and hypopituitarism symptoms resulting from compression of the anterior pituitary. In some pituitary masses, symptoms of increased intracranial pressure (e.g., headache, nausea, vomiting, and papilledema) may be observed, though they are less common. RCC is classified as a non-functional tumor because it is not associated with hormone hypersecretion. As a result, the clinical presentation is predominantly related to the mass effect from the tumor pressing on adjacent structures.[ 3 , 13 ]

Endonasal Transsphenoidal Surgery is a commonly used minimally invasive procedure for the removal of suprasellar pituitary tumors. This approach is advantageous because it avoids external incisions, reduces the risk of complications, and promotes faster recovery. Anesthesia in this procedure focuses on two main goals: Protection of the brain, ensuring stable cerebral perfusion and function during surgery. Facilitation of the surgical area, which involves controlling intracranial pressure and brain volume to reduce the risk of secondary brain injury. Various techniques are employed to optimize the surgical environment: For large tumors, a lumbar intrathecal catheter (lumbar drain) may be placed. This allows for the drainage of cerebrospinal fluid (CSF) or the infusion of isotonic saline, which can help maneuver the pituitary during the procedure. This can provide better access to the tumor by temporarily altering the position of the pituitary gland. These approaches help create a safer surgical space and minimize risks associated with brain tissue pressure during the operation.[ 12 ]

Evaluation of urine production is crucial during surgery to anticipate dehydration and adjust fluid management. In this case, polyuria was observed within the first hour of surgery, with a urine output of 21.25 mL/kgbw/h. To address this, crystalloid fluid replacement was administered. Patients with a history of polyuria, particularly those with suprasellar tumors, may develop central diabetes insipidus (DI), which is commonly caused by damage to the pituitary gland or hypothalamus (Hawkes et al., 2019).[ 10 ] Although intravenous vasopressin is typically used for DI, it was not available in this case. Desmopressin, an ADH analog, is generally available as an oral regimen but is difficult to administer during surgery. Oxytocin, which shares a similar structure with vasopressin, is sometimes used as an alternative to manage central DI. Despite the controversial nature of this treatment, oxytocin (10–20 mU/min) has been reported to exert an antidiuretic effect in cases of central DI. In this patient, continuous oxytocin administration during surgery successfully normalized urine output.[ 2 , 4 , 8 , 9 ]

Postoperative care in the ICU focuses on maintaining fluid balance and preventing electrolyte imbalances, especially in patients with a history of central diabetes insipidus (DI), such as in this case.

Key goals include: Fluid replacement: The main objective is to replace the fluids lost through urine production to prevent dehydration. Sodium balance: Plasma sodium levels should be monitored and maintained within a safe range. It’s important to correct sodium levels gradually, with a maximum reduction rate of 1 mEq/h and 10 mEq/day to avoid complications such as cerebral edema or seizures. Patients who are unconscious or have impaired thirst mechanisms will require intravenous fluid therapy along with pharmacologic treatments to support hydration and ensure plasma sodium balance. Regular monitoring of serum sodium levels and other electrolytes is critical to guide adjustments in fluid management. This approach helps to stabilize the patient postoperatively and reduces the risk of complications related to fluid and electrolyte imbalances.

DI is a condition characterized by a failure in the ADH (antidiuretic hormone) homeostasis process, often due to dysfunction in the hypothalamic-pituitary axis, particularly in the suprasellar region. The clinical manifestations of DI typically include: Polyuria: Urine output exceeding 2 cc/kg body weight per hour for at least 3 consecutive hours. Low urinary osmolarity: Decreased urinary osmolarity (e.g., 279.3 mmol/kg in this case), which is significantly lower than normal (below 350 mmol/kg). Low urine specific gravity: A specific gravity around 1.001, which is very dilute and typical of DI. High plasma osmolarity: Plasma osmolarity may increase (e.g., 331 mmol/kg), reflecting dehydration due to impaired water reabsorption. Absence of other conditions: There should be no excess fluid intake, no diuretic therapy influence, and no evidence of intrarenal abnormalities.[ 6 ] In the postoperative management of DI, desmopressin (an ADH analog) is used to treat the condition. In this case, the initial dose of desmopressin was 1 × 0.05 mg. Careful monitoring of electrolytes during treatment is essential to prevent complications. Since the patient was conscious and able to drink fluids, oral hydration was encouraged to help manage the increased urine output and prevent further dehydration, thus preventing worsening of the condition. Continuous monitoring of the patient’s fluid balance, electrolyte levels, and urine output remains essential to ensure proper hydration and balance during recovery.

CONCLUSION

In this case, Diabetes Insipidus (DI) is identified as a failure in the ADH (antidiuretic hormone) homeostasis process due to dysfunction in the hypothalamic-pituitary axis, specifically in the suprasellar region. The Rathke cleft cyst (RCC), a nonfunctional pituitary tumor, can disrupt normal pituitary function postoperatively, impairing the secretion of ADH. This disruption leads to central DI, characterized by excessive urine production (polyuria), which increases the risk of dehydration and electrolyte imbalances, particularly hypernatremia. Postoperative management in the ICU is focused on maintaining fluid balance. This involves: Replacing lost fluids due to excessive urine production. Desmopressin therapy as an ADH analog to control the diuresis process and reduce urine output. Electrolyte monitoring to prevent imbalances, particularly the risk of hypernatremia due to dehydration. The management of Rathke cleft cyst (RCC) and Diabetes Insipidus (DI) in pediatric patients requires a multidisciplinary approach throughout the preoperative, intraoperative, and postoperative phases, involving a combination of endocrinologists, pediatricians, neurosurgeons, and anesthesiologists to ensure optimal care and recovery.

Ethical approval:

The Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of Interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Disclaimer

The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.

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